CDKN2A and chordoma: Earlier studies employing microarray technologies, fluorescence in situ hybridization, quantitative PCR, and targeted sequencing of select cancer genes showed that chordomas are primarily characterized by non-random DNA copy number losses across the genome, frequently involving CDKN2A, PTEN, and chromatin regulatory genes such as SMARCB1 as potentially actionable alterations, as well as recurrent gains of the TBXT gene encoding brachyury6–9.